ArticleBiology open2013
Myosin IIA deficient cells migrate efficiently despite reduced traction forces at cell periphery.
Article in Biology open, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
29 citing papers in PubMed, 38 citations in OpenAlex.
- Talin2 binds to non-muscle myosin IIa and regulates cell attachment and fibronectin secretion.Scientific reports · 2024Article
- Review
- From stress fiber to focal adhesion: a role of actin crosslinkers in force transmission.Frontiers in cell and developmental biology · 2024Review
- Extracellular matrix composition alters endothelial force transmission.American journal of physiology. Cell physiology · 2023Article
- Extracellular Matrix Composition Alters Endothelial Force Transmission.Research square · 2023Article
- An Easy-to-Fabricate Cell Stretcher Reveals Density-Dependent Mechanical Regulation of Collective Cell Movements in Epithelia.Cellular and molecular bioengineering · 2021Article
- Article
- An asymmetric junctional mechanoresponse coordinates mitotic rounding with epithelial integrity.The Journal of cell biology · 2021Article
- A novel method for sensor-based quantification of single/multicellular force dynamics and stiffening in 3D matrices.Science advances · 2021Article
- Myosin II isoforms play distinct roles ineLife · 2019Article
- Myosin IIA-mediated forces regulate multicellular integrity during vascular sprouting.Molecular biology of the cell · 2019Article
- Rab6 regulates cell migration and invasion by recruiting Cdc42 and modulating its activity.Cellular and molecular life sciences : CMLS · 2019Article
- Nonmuscle myosin IIA and IIB differentially modulate migration and alter gene expression in primary mouse tumorigenic cells.Molecular biology of the cell · 2019Article
- Myosin-18B Promotes the Assembly of Myosin II Stacks for Maturation of Contractile Actomyosin Bundles.Current biology : CB · 2019Article
- Article
- Different contributions of nonmuscle myosin IIA and IIB to the organization of stress fiber subtypes in fibroblasts.Molecular biology of the cell · 2018Article
- UNC-45a promotes myosin folding and stress fiber assembly.The Journal of cell biology · 2017Article
- Self-sorting of nonmuscle myosins IIA and IIB polarizes the cytoskeleton and modulates cell motility.The Journal of cell biology · 2017Article
- Myosin IIA Heavy Chain Phosphorylation Mediates Adhesion Maturation and Protrusion in Three Dimensions.The Journal of biological chemistry · 2017Article
- Cellular microenvironment modulates the galvanotaxis of brain tumor initiating cells.Scientific reports · 2016Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Cell motility is a cornerstone of embryogenesis, tissue remodeling and repair, and cancer cell invasion. It is generally thought that migrating cells grab and exert traction force onto the extracellular matrix in order to pull the cell body forward. While previous studies have shown that myosin II deficient cells migrate efficiently, whether these cells exert traction forces during cell migration in the absence of the major contractile machinery is currently unknown. Using an array of micron-sized pillars as a force sensor and shRNA specific to each myosin II isoform (A and B), we analyzed how myosin IIA and IIB individually regulate cell migration and traction force generation. Myosin IIA and IIB localized preferentially to the leading edge where traction force was greatest, and the trailing edge, respectively. When individual myosin II isoforms were depleted by shRNA, myosin IIA deficient cells lost actin stress fibers and focal adhesions, whereas myosin IIB deficient cells maintained similar actin organization and focal adhesions as wild-type cells. Interestingly, myosin IIA deficient cells migrated faster than wild-type or myosin IIB deficient cells on both a rigid surface and a pillar array, yet myosin IIA deficient cells exerted significantly less traction force at the leading edge than wild-type or myosin IIB deficient cells. These results suggest that, in the absence of myosin IIA mediated force-generating machinery, cells move with minimal traction forces at the cell periphery, thus demonstrating the remarkable ability of cells to adapt and migrate.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.